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神经细胞NCAM及TGF-β2在脑胶质瘤中表达的意义 总被引:1,自引:0,他引:1
目的 研究神经细胞黏附分子 ( NCAM)、转化生长因子β2 ( TGF-β2 )在胶质瘤中的表达。方法 采用免疫组化 ( Envision)二步法 ,对 71例脑胶质瘤及 6例正常脑组织进行研究。对所有入选病例均进行随访。结果 TGF-β2在正常脑组织中未见表达 ,NCAM在正常脑组织中高表达 ,两者在胶质瘤细胞中均有不同程度的表达 ,表达强度与肿瘤的恶性程度相关。 NCAM与 TGF-β2 表达呈负相关 ( P<0 .0 5 )。生存率统计表明 NCAM、TGF-β2 表达不同的组间 3年生存率差异均有显著性。结论 NCAM及 TGF-β2 在不同病理级别胶质瘤表达差异有显著性 ,NCAM反映肿瘤侵袭性 ,TGF-β2 反映肿瘤的恶性生物学行为 ,两者均可作为病理分级辅助手段评估胶质瘤患者预后 相似文献
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人脑胶质瘤组织中nm23与PCNA的表达及其意义 总被引:2,自引:0,他引:2
背景与目的:脑胶质瘤极少发生颅外转移,死亡的主要原因是肿瘤的原位复发,因此,通过检测基因表达进一步了解其生物学特性很重要。本研究旨在探讨胶质瘤组织中肿瘤转移抑制基因(non-metastasis,nm23)、增殖细胞核抗原(proliferatingcellnuclearantigen,PCNA)的表达及其对肿瘤恶性程度的判断、患者预后评估和复发预测的意义。方法:用免疫组化SP法测定50例不同恶性程度的胶质瘤组织中nm23、PCNA的表达情况。结果:(1)低度恶性胶质瘤标记指数(labelindex,LI)nm23为3.40±0.27,PCNA为3.60±0.05;高度恶性胶质瘤nm23LI为1.72±0.18,PCNALI为6.20±0.23,有显著性差异(P<0.05);(2)25例低度恶性胶质瘤中nm23阳性14例(56%),PCNA阳性16例(64%);而25例高度恶性胶质瘤中nm23阳性3例(12%),PCNA阳性22例(88%)。低度和高度恶性胶质瘤两组nm23、PCNA表达阳性率有显著性差异(P<0.05);(3)复发组9例,无nm23阳性者(0%),PCNA全部阳性(100%),未复发组8例,4例nm23阳性(50%),4例PCNA阳性(50%),两组nm23、PCNA的表达阳性率均有显著性差异(P<0.05);(4)胶质瘤nm23与PCNA的标记指数呈负相关(r=-0.5335,P<0.001)。结论:(1)nm23的表达随胶质瘤恶性程度增加而下降;(2)PCNA的表达随胶质瘤恶性程度的增加而升高;(3)nm23、PCNA可作为胶质瘤恶 相似文献
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目的:探讨胶质瘤细胞egr-1基因表达水平与肿瘤恶性程度、细胞增殖活性及凋亡程度的关系。方法:用原位杂交、原位细胞凋亡检测和免疫组化染色方法观察了73例不同级别的胶质瘤。结果:73例胶质瘤egr-1mRNA和EGR-1蛋白阳性表达率均为100%.这两种阳性肿瘤细胞密度均随肿瘤恶性程度升高而相应增加,不同级别组间比较差异均有显著性(P〈0.01)。73例胶质瘤增殖细胞核抗原(PCNA)阳性肿瘤细胞和凋亡肿瘤细胞检出率均为100%。随肿瘤恶性程度升高,PCNA阳性肿瘤细胞密度增加而凋亡肿瘤细胞密度减少,不同级别组间比较差异均有显著性(心0.05~0.01)。经直线相关分析证实,egr-1mRNA、EGR-1蛋白和PCNA阳性肿瘤细胞密度彼此间均呈显著性正相关(r=0.685~0.999,P〈0.01),前三种阳性肿瘤细胞密度均与凋亡肿瘤细胞密度呈显著性负相关(r=-0.758—0.775,P〈0.01)。结论:egr-1基因表达水平对评价胶质瘤生物学行为有重要参考价值。胶质瘤细胞egr-1基因表达异常增加可能是促进肿瘤细胞增殖和抑制其凋亡的重要因素,并在胶质瘤发生及恶性进展过程中均起重要作用。 相似文献
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目的探讨TGF-β1、p53、PTEN蛋白在不同恶性程度胶质瘤中的表达及临床意义.方法应用免疫组化EliVisionTM二步法检测92例胶质瘤中TGF-β1、p53、PTEN蛋白的表达.结果 TGF-β1、p53与胶质瘤级别呈正相关,高分化组与低分化组组间差异有显著性(P<0.05、P<0.01);PTEN与胶质瘤级别呈负相关,高分化组与低分化组组间差异有显著性(P<0.05);TGF-β1与p53的表达呈正相关(r=0.231、P<0.05);PTEN不表达、p53表达的胶质瘤患者预后差(P<0.05、P<0.05).结论 PTEN、p53的表达与预后密切相关,可以作为判断胶质瘤预后的标记. 相似文献
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目的:检测人脑恶性胶质瘤组织中IL13Rα2和增殖细胞核抗原(proliferating cell nuclear antigen, PCNA)的表达强度,分析其与患者临床病理特点和预后之间的关系。方法:选取20022006年温州医学院附属第一医院手术治疗的43例恶性胶质瘤标本;采用免疫组织化学法检测并用图像分析系统分析IL13Rα2和PCNA在恶性胶质瘤组织中的表达,分析两者间的相关性;分析它们与临床特征和预后的关系。结果:(1) 43例恶性胶质瘤标本有40例(93%)IL13Rα2阳性表达和36例(84%)PCNA阳性表达;(2) IL13Rα2和PCNA表达强度与肿瘤部位和肿瘤大小无相关性(P>0.05);在WHOⅢ级与Ⅳ级间两者表达强度差异均有统计学意义(P=0.031, P=0.002);在生存时间≤6个月与>6个月患者间IL13Rα2 表达强度差异有统计学意义(P=0.028)。(3)IL13Rα2和PCNA的表达强度呈显著的正相关(r=0.653,P=0.000)。结论:人恶性胶质瘤组织中IL13Rα2和PCNA均高表达,前者表达强度与肿瘤恶性分级和患者预后密切相关,在恶性胶质瘤的诊断和预后判断中具有潜在的临床应用价值。 相似文献
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细胞骨架蛋白tubulin α、β在不同级别胶质瘤中的表达及其与预后的相关性 总被引:1,自引:0,他引:1
目的探讨不同病理学分级胶质瘤中细胞骨架蛋白tubulin α、β的表达,评估tubulin α、β表达水平与胶质瘤的恶性程度及其与预后的相关性.方法应用免疫组化方法检测57例不同病理级别人胶质瘤组织中tubulin α、β表达情况,并分析tubulin α、β表达水平与病理分级及患者术后生存时间的相关性.结果不同级别胶质瘤tubulin α、β表达水平不同,高级别(Ⅲ、Ⅳ级)与低级别(Ⅰ、Ⅱ级)胶质瘤tubulin α、β表达水平的差异有显著性(P〈0.05),且tubulin α、β表达水平与患者术后生存时间呈正相关性.结论 tubulin α、β在胶质瘤恶性进展方面可能具有重要意义,对指导胶质瘤的分期、组织学分级和判断患者的预后有一定参考价值. 相似文献
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目的 探讨胶质瘤组织中转化生长因子-β1(TGF-β1)和CD105蛋白表达的相互关系及其临床意义。方法 应用免疫组化SP法检测70例胶质瘤和10例正常脑组织中TGF-β1和CD105的表达水平,并分析它们与胶质瘤临床病理因素的关系。结果 TGF-β1和CD105表达均与胶质瘤病理分级相关(P〈0.01),与患者的性别、年龄及肿瘤大小无明显关系(P〉0.05)。TGF-β1阳性表达组的MVD(37.68±4.91)显著高于阴性表达组(30.01±5.26),(P〈0.01),且TGF-131表达与CD105-MVD呈正相关(r=0.6547,P〈0.05)。结论 TGF-β1和CD105高表达共同促进胶质瘤恶性增殖与血管形成。 相似文献
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干细胞标志物CD133和Nestin在不同恶性程度胶质瘤组织中的表达及其与预后的关系 总被引:1,自引:0,他引:1
背景与目的:近来研究表明,胶质瘤中一小群表达干细胞标志的细胞是胶质瘤发生及发展的根源。本文探讨干细胞标志物CD133和Nestin在不同恶性程度人脑胶质瘤组织中的表达情况及其与预后的关系。方法:应用实时荧光定量PCR方法定量检测77例不同恶性程度胶质瘤组织中CD133和Nestin基因的表达情况,并与肿瘤的恶性程度进行相关分析;探讨肿瘤组织中上述基因的表达水平与患者预后的关系。结果:在不同恶性程度胶质瘤组织中,CD133及Nestin的表达存在显著性差异(P〈0.05),CD133和Nestin的表达情况与肿瘤的恶性程度呈正性相关(P〈0.05);单因素预后分析显示CD133和Nestin的表达水平与预后相关(P〈0.05),CD133和Nestin基因的高表达预示一个较短的生存时间;多因素Cox比例风险回归模型分析显示,CD133是独立于病理级别及其他临床变量的预后因子。结论:检测胶质瘤组织中CD133和Nestin的表达水平有助于评价肿瘤的生物学行为和患者的预后。 相似文献
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目的:探讨胶质瘤p^27Kipl,bcl-2和PCNA蛋白表达与肿瘤恶性程度、细胞增殖活性、凋亡程度的关系。声去采用免疫组化染色S-P法检测66例不同级别的胶质瘤p^27Kipl,bcl-2和PCNA蛋白的表达。结果:在66例胶质瘤甲,p^27Kipl表达18例(27%),bcl-2表达20例(30%),PCNA表达51例(77%)。p^27Kipl蛋白表达率随着胶质瘤级别升高而减少.bcl-2蛋白表达率随肿瘤级别升高而相应增加;PCNA表达随胶质瘤级别升高阳性反应强度增加;但Ⅰ、Ⅱ与Ⅲ级和Ⅳ级组间无显著性差异。结论:p^27Kipl蛋白表达的缺失可能与胶质瘤的发生有关;bcl-2基因可能间接抑制细胞凋亡而与胶质瘤的分型、细胞的增殖活性以及潜在的临床行为无直接关系;PCNA的表达与星形胶质细胞瘤的恶性行为有关。 相似文献
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背景与目的:之前已有研究证明,整合素参与调节细胞多种生物学效应;黏着斑激酶(FAK)、细胞外调节蛋白激酶(ERK1/2)蛋白表达及磷酸化的水平与胶质瘤细胞恶性程度及其诊断、预后密切相关。本研究通过检测整合素αvβ3拮抗剂IS201对人GL15胶质瘤细胞FAK、ERK1/2蛋白表达及其磷酸化的影响,探讨其意义。方法:用不同浓度的整合素αvβ3拮抗剂IS201处理GL15细胞,用Western印迹法检测细胞的FAK、ERK1/2表达量以及FAK、ERK1/2的磷酸化程度。结果:各实验组不同浓度的IS201均能明显降低FAK、ERK1/2的表达,对FAK、ERK1/2的磷酸化有明显的抑制作用。各实验组差异均具有统计学意义(P〈0.05)。结论:IS201对人GL15胶质瘤细胞FAK、ERK1/2蛋白表达量及其磷酸化均起负性调节作用,对胶质瘤的细胞增殖和侵袭性生长等恶性生物学行为起抑制作用。 相似文献
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Cheryl L. Holt PhD Robert A. Oster PhD Kimberly S. Clay PhD Julie Urmie PhD Mona Fouad MD MPH 《Journal of psychosocial oncology》2013,31(4):372-393
The literature suggests that religiosity helps cope with illness. The present study examined the role of religiosity in functioning among African Americans and Whites with a cancer diagnosis. Patients were recruited from an existing study and mailed a religiosity survey. Participants (N = 269; 36% African American, 56% women) completed the mail survey, and interview data from the larger cohort was utilized in the analysis. Multivariate analyses indicated that in the overall sample religious behaviors were marginally and positively associated with mental health and negatively with depressive symptoms. Among women, religious behaviors were positively associated with mental health and negatively with depressive symptoms. Religiosity was not a predictor of study outcomes for men. Among African Americans, religious behaviors were positively associated with mental health and vitality. Among Whites, religious behaviors were negatively associated with depressive symptoms. These findings suggest a mixed role of religious involvement in cancer outcomes. The current findings may have applied potential in the areas of emotional functioning and depression. 相似文献
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Epidemiologic evidence on the relation between occupational and environmental radiation and cancer is reviewed. Studies of pioneering radiation workers, underground miners, and radium dial painters revealed excess cancer deaths and contributed to the setting of radiation protection standards and to theories of carcinogenesis. Occupational exposures today are generally much lower than in the past, thus any associated increases in cancer will be difficult to detect. Pooling investigations of these more recently exposed workers, however, has the potential to validate current estimates of risk used in radiation protection. New information on the effects of chronic radiation exposure also may come from studies in the former Soviet Union of Chernobyl clean-up workers and of workers at the Mayak nuclear facilities. Studies of environmental radiation exposures, other than radon, are largely inconclusive, due mainly to the difficulties in detecting the low risks associated with low dose exposures. Thyroid cancer, however, has been linked to environmental radiation from the Chernobyl accident and from nuclear weapons tests. Low-level radiation released during normal operations at nuclear plants has not been found to increase cancer rates in surrounding populations. Radon, a human carcinogen, is the most ubiquitous exposure to human populations; remediating high residential-radon levels is recommended, recognizing that the exposure can never be removed completely because it occurs naturally. 相似文献
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New and emerging radiosensitizers and radioprotectors 总被引:3,自引:0,他引:3
The combination of chemotherapy and radiation has led to clinical breakthroughs in several disease sites, and current work continues to define optimum combinations of proven chemotherapy as well as more recently available, noncytotoxic agents. Administration of systemic therapies allows modulation of radiation response to improve tumor control (radiosensitization) or to prevent normal tissue toxicity (radioprotection). Substantial progress has been made in identifying the targets of standard chemotherapeutic radiation sensitizers and protectors as well as in the introduction of a new generation of molecularly targeted therapies in combination with radiation. We have reviewed the most recent, predominantly early phase clinical trials combining systemic agents with radiation. Although the proof of an improved schedule ultimately needs to come from well-run Phase III trials, the search among schedules could be shortened by the use of surrogate endpoints such as presence of active drug metabolites in the tumor. This has been accomplished only in a few cases and needs to become a more standard part of radiation sensitizer and protector trials. 相似文献
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Key TJ 《British journal of cancer》2011,104(1):6-11
The possibility that fruit and vegetables may help to reduce the risk of cancer has been studied for over 30 years, but no protective effects have been firmly established. For cancers of the upper gastrointestinal tract, epidemiological studies have generally observed that people with a relatively high intake of fruit and vegetables have a moderately reduced risk, but these observations must be interpreted cautiously because of potential confounding by smoking and alcohol. For lung cancer, recent large prospective analyses with detailed adjustment for smoking have not shown a convincing association between fruit and vegetable intake and reduced risk. For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. It is still possible that there are benefits to be identified: there could be benefits in populations with low average intakes of fruit and vegetables, such that those eating moderate amounts have a lower cancer risk than those eating very low amounts, and there could also be effects of particular nutrients in certain fruits and vegetables, as fruit and vegetables have very varied composition. Nutritional principles indicate that healthy diets should include at least moderate amounts of fruit and vegetables, but the available data suggest that general increases in fruit and vegetable intake would not have much effect on cancer rates, at least in well-nourished populations. Current advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put most emphasis on the well-established adverse effects of obesity and high alcohol intakes. 相似文献
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目的:探讨VEGF和KDR在大肠腺瘤和大肠腺癌中的表达及临床病理特征的关系。方法:大肠腺瘤和大肠腺癌组织标本各100例,采用免疫组织化学染色法检测VEGF和KDR在标本中的表达情况。结果:VEGF和KDR在大肠腺癌组中的阳性表达明显高于大肠腺瘤组(P〈0.05);在正常大肠黏膜均未见VEGF和KDR表达的阳性染色;VEGF阳性表达组中KDR的阳性表达率为70%,显著高于VEGF阴性表达组中KDR的阳性表达率16%,两组比较有统计学意义(P〈0.01)。结论:大肠腺癌组织中KDR的表达与肿瘤大小、转移情况、浸润深度密切相关;VEGF和KDR在大肠腺瘤中的表达与患者的年龄、性别及分型均无相关性,而与增生程度相关(P〈0.05)。在大肠腺癌患者中VEGF及KDR表达更高,二者具有协同效应。 相似文献
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《European journal of cancer (Oxford, England : 1990)》2014,50(15):2649-2658
Vitamin D is formed mainly in the skin upon exposure to sunlight and can as well be taken orally with food or through supplements. While sun exposure is a known risk factor for skin cancer development, vitamin D exerts anti-proliferative and pro-apoptotic effects on melanocytes and keratinocytes in vitro. To clarify the role of vitamin D in skin carcinogenesis, we performed a review of the literature and meta-analysis to evaluate the association of vitamin D serum levels and dietary intake with cutaneous melanoma (CM) and non-melanoma skin cancer (NMSC) risk and melanoma prognostic factors. Twenty papers were included for an overall 1420 CM and 2317 NMSC. The summary relative risks (SRRs) from random effects models for the association of highest versus lowest vitamin D serum levels was 1.46 (95% confidence interval (CI) 0.60–3.53) and 1.64 (95% CI 1.02–2.65) for CM and NMSC, respectively. The SRR for the highest versus lowest quintile of vitamin D intake was 0.86 (95% CI 0.63–1.13) for CM and 1.03 (95% CI 0.95–1.13) for NMSC. Data were suggestive of an inverse association between vitamin D blood levels and CM thickness at diagnosis. Further research is needed to investigate the effect of vitamin D on skin cancer risk in populations with different exposure to sunlight and dietary habits, and to evaluate whether vitamin D supplementation is effective in improving CM survival. 相似文献
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Tarin D 《Seminars in cancer biology》2011,21(2):72-82
This review describes a new vision for future directions in the study of metastatic cancer biology and pathology. It is based upon clinical and experimental observations on the constituent cell lineages within a neoplasm and on tumour-host interactions. The vision incorporates information from studies in population biology, developmental biology and experimental pathology as well as investigations upon human malignant disease. The assembled information reveals that invasion and metastasis are supra-cellular manifestations of "emergent behavior" among combinations of normal and malignant cell lineages in vivo. Emergent behavior is a combinatorial interactive process in which a population displays new traits which cannot be achieved by individuals acting separately and which subside when the specific population mix disaggregates. Disruption of such pathological interactions in the field of a developing primary or secondary tumour is, therefore, required to disable the malignant population and arrest progression without tissue destruction. These conclusions originate, in part, from principles which govern the sociobiology and group behavior of bees, ants, fish, birds and human societies. In all these social organisms, external factors can disrupt signaling mechanisms and induce expanding self-perpetuating rogue behavior, leading to social disintegration. These principles also apply to cellular societies composing higher animals, which likewise need intrinsic rules to maintain social order and avoid anarchy, and recognition of this is essential for advancing future research on the mechanisms involved in carcinogenesis and metastasis. Summarised evidence is presented here to support the conclusion that miscommunications between cells and tissues in the region of the developing tumour and its metastases are the main direct perpetrators of malignant disease. Genetic lesions (mutations, deletions, translocations, reduplications, etc.), commonly seen in cancers, can significantly disrupt important molecular pathways in the networks of communications needed to sustain orderly tissue/organ structure and function. However, genetic lesions can also, themselves, be induced by abnormal cell interactions initiated by extrinsic carcinogenic agents such as chemicals, viruses, hormones and radiation. The evidence shows that, irrespective of the initiating cause, it is this miscommunication in the region of a developing tumour and its metastases that is ultimately responsible for the emergence and progression of the disease. The article describes how this information collectively, provides a framework for designing specific novel therapeutic approaches targeting the cell and tissue interactions driving tumour metastasis and its manifold effects on the whole body. 相似文献